The response of spleen dendritic cell-enriched population to bacterial and allogeneic antigens.
The dendritic cells (DC) play crucial role in initiation and modulation of immune response especially innate immune response. We investigated the influence bacterial (E. coli and S. epidermidis) and allogeneic antigens (heart, skin and bone marrow transplants) on splenic DC- enriched population. We found that 1) the in culture stimulation of rat splenic DC-enriched population by E. coli, S.epidermidis, LPS and CpG DNA caused increase in class II-positive cells. Simultaneously, a decrease in percentage of EDI, B cells and OX62 migrating DC upon treatment with S.epidermidis was observed. LPS caused decreased frequency of OX62 and NK cells. 2) Similarly to the in vitro the in vivo stimulation by E. coli, S.epidermidis, LPS and CpG DNA increased the percentage of class II-positive cells. There was a decrease in the ED1, OX62 and B cell populations following stimulation by S. epidermidis. 3) Mixed DC-enriched population and donor PBM culture showed high level of response in both populations. 4) Syngeneic and allogeneic transplants of heart, skin and BMC caused increase in class II-positive cells. Moreover, there was an increase in frequency of the ED1 and W3/13 populations after both syn- and allogeneic transplantation. The OX62 cells did not react, whereas the B cell frequency rose only after allogeneic transplantation. A significant decrease in NK cell population was noticed. 5) The in vitro and in vivo bacterial stimulation brought about expression of TLR receptors and Hsp. Mixed recipient DC with donor PBM culture caused expression of Hsp 90 but not TLRs. Allogeneic stimulation by transplanted tissues did not evoke expression of the investigated receptors and proteins. 6) Recipient DC-enriched population produced IFN gamma upon stimulation with bacteria and skin but not heart and BMC. Further studies on simultaneous stimulation of splenic DCs by bacterial and allo-antigens will throw light on additive effects of bacterial activation in allograft rejection.